NIH
scientist Dr. Julius Axelrod used the SPF to measure
tiny amounts of serotonin in the blood. Serotonin
was first isolated from the blood in 1948 and
identified as being present in the central nervous
system. The body system involving serotonin is
known to affect mood, emotion, sleep, and appetite.
One cause of depression is an abnormal function
of the serotonin transmitter system. Therefore,
a drug that builds the concentrations of serotonin
should alleviate the symptoms.

Dr.
Axelrod's research, for which he won the
Nobel Prize in 1970, led to the development
of SSRI (selective serotonin re-uptake inhibitor)
drugs such as Prozac, Zoloft, and Paxil.

How
does an SSRI work?
The brain is made up of neurons, which are interconnected
brain cells. Messages travel along these cells.
When a message reaches the end of a neuron, it has
to jump a gap (called a synapse) to the next one.
To do this, the neuron releases tiny amounts of
a chemical (a neurotransmitter) into the gap between
the nerve cells. Ideally, a nerve impulse starts
in the new nerve, and thus the message gets from
one nerve to the next. In order for the original
nerve to recover and get the next message, it needs
to replace its stocks of the neurotransmitter in
the original neuron so it is ready to send the next
message. The "healthy" body thus takes
the neurotransmitter back into the originating neuron
(this is called "re-uptake").

In
the case of depression, certain neurotransmitters
such as serotonin are lacking, so they cannot
be taken back in full to the originating neuron
and therefore cannot send the next message. SSRIs
slow down the process of returning serotonin to
the end of the neuron it comes from (they inhibit
the process of re-uptake). This makes it more
likely that enough serotonin will build up to
set off the impulse in the next neuron. Therefore,
SSRIs work by allowing the body to make the best
use of reduced amounts of serotonin.